Skin conditions in wrestling – how to prevent

Krisztián Gáspár, MD, PhD Assistant professor University of Debrecen Faculty of Medicine Department of Dermatology Debrecen, Hungary Disclosure

• Presenter: Krisztián Gáspár

• I have the Relationships with commercial interests: – Advisory Board/Speakers Bureau: none – Funding (Grants/Honoraria): none – Research/Clinical Trials: Eli Lilly, Novartis, Pfizer, Janssen, Sanofi, Abbvie – Speaker/Consulting Fees: Eli Lilly, Novartis, Janssen, Sanofi, Abbvie

• None to disclose regarding this presentation

Objectives

• Normal and impaired skin barrier

• Atopic dermatitis – model for understanding barrier

• Skin diseases in wrestling

• Treatments

• Prevention techniques in skin infections

Skin barrier

Danger model: ”The basic function of immune system is not to distinct between self and non-self, but to recognize danger”

Polly Matzinger, PhD, Immunologist, NIH

In order to avoid or prevent a loss on the mat you need a good defense –

The same is true for skin (an active defense) Skin barrier functions

Physicochemical barrier and immunological barrier – in close morphological and functional connection

Physicochemical barrier Immunological barrier (SIS)

 Stratum corneum: corneocytes • Epidermis, dermis  Stratum granulosum: keratinocytes • Keratinocytes, dendritic cells, T cells  Cornified envelop , structural proteins • Defensins, cytokines, chemokines (filaggrin)  Lipid layer, proteases, protease inhibitors, defensins  Tight junctions, corneodesmosomes Physicochemical barrier

Genetics

Environmental factors - microbes (viruses, fungi, bacteria, parasites) - physical factors (e.g. UV, humidity, scratching) - chemicals (e.g. irritants) - biological factors (allergens)

http://crmsnchrysnths.blogspot.com/2017/09/what-is-skin-barrier.html Elements of intact physicochemical barrier

Barrier: Cells: corneocytes Intercellular junctions: corneodesmosomes Intercellular matrix: lipids, enzymes

https://www.sheffield.ac.uk/iicd/research/rr/dermatology/skinbarrierfacility Five major groups of skin barrier genes

Enzymes having role in desquamation and cross-linking Tight junction KLK7 KLK5 KLK14 components TGM1 TGM3 TGM5 CLDN1 CLDN16 CLDN23 Barrier structure components OCLN Keratins: Other KRT1 molecules: KRT10 FLG KRT6 LOR Corneodesmosome KRT16 PPL components KRT17 SPRR1A CDH1 DSG1 KRT79 SPRR2A DSC1 PKP1 LCE1F CDSN LCE1D Antimicrobial peptides (AMPs) S100A7 S100A8 S100A9 DEFB4B LCN2 TSLP Impaired physicochemical barrier

http://crmsnchrysnths.blogspot.com/2017/09/what-is-skin-barrier.html

Current Dermatology Reports December 2018, Volume 7, Issue 4, pp 209–220 Skin Barrier Function and Atopic Dermatitis Consequences of impaired barrier

Increased penetration of Increased transepidermal allergens, irritants, pathogens waterloss (TEWL)

+ increased KC and LC activity that leads to increased immunbarrier activity

Inflammation

Hudson TJ Nature Genetics 2006 Immunological barrier

ADAPTIVE immune response INNATE immune response Slowly developing  Antigen specific Immediate reaction  Transferrable to Not antigen specific another host Not transferrable No immunmemory  Immunmemory exists  Exponential empowering Major elements of cutaneous immune responses

Innate immune response Adaptive immune response Cellular Phagocytes (macrophages, granulocytes) T lymphocytes elements Dendritic cells B lymphocytes NK cells Keratinocytes Endothelial cells Humoral Complement system Antibodies elements Cytokines Interleukins chemokines (cytokines) C-reactive protein Mannose-binding lectin Lipopolisacharide-binding protein Antimicrobial peptids etc. Skin as an immune organ

Resident skin immune cells Impaired immunological barrier

Good model of impaired physicochemical and immunological barrier Inflamm Regen. 2017 Jun 5;37:14. doi: 10.1186/s41232-017-0044-7. Pathogenesis of AD

Genetic factors (mutations, epigenetics) Close and not independent connection Decreased level of FLG Skin infections, low and structure proteins between the pDC, PMN cell count in skin abnormalities of epidermal Innate and Skin barrier barrier Adaptive changes, dry Immune system skin, mechanic function and changes trauma immunological

Sensitization, Proinflammatory cytokines mechanisms, Leukocyte recruitment and chemokines with genetic and activation (TSLP, IL-16, TNFa, CCL26, CCL27) and

Hygiene hypothesis – soaps, environmental Hygiene hypothesis – Impaired detergents in barrier impairment Th1/Th2 balance and Treg function changes in the Environmental factors background (allergens, irritants, microbes, stress) Atopic Dermatitis

• Chronic, non-contagious inflammatory skin disease.

• Dry skin, pruritus, possible superinfections (>90% S. aureus colonization).

• Prevalence in Europe in children 15-25%, in adults 2-10%, continuously increasing. Skin barrier prevention – levels of prevention

• Primary prevention: healthy person

• Secondary prevention: atopic, symptom free (+atopy march)

• Tertiary prevention: atopic, chronic patient

Prevention techniques – possibilities

• Avoidance mechanisms (specific and non- specific triggers, provocation factors) (?)

• Diet, probiotics

• Continuous emollient use

Simpson et al JACI 2014 The First: open-label, prospective study

High AD-risk children: 30-50% development of AD in first 2 years

22 high AD-risk newborns Emollient therapy From week 1 for 2 years (2006-2008) Daily at least 1x (QD)

15 % developed disease

Transepidermal waterloss (TEWL) decreased

Simpson E et al. JAAD 2010 The First: Randomized, controlled study

124 high AD-risk newborns (108 finished study) Emollient therapy (oil, cream, ointment) from M1 for 6 months (2010-2011) Daily at least 1x In control group no emollient

Emollient use well tolerated by patients

AD cumulative incidence (50% drop): emollient group 22%, control group 44%

Therapy adherence high

Simpson E et al. JACI 2014 Prospective, randomized, controlled trial

118 high AD-risk newborns Emollient therapy from M1 for 32 weeks (2010-2013) Daily at least 1x In control group no emollient

AD cumulative incidence dropped by 33%

Horimukai et al. JACI 2014 New clinical studies

Higher patient number More frequent use AD incidence? Presence of sensitization? Longer trials

Why important to restore the barrier? Basic treatment

• Complex treatment in AD is unavoidable and inevitable in both acute and chronic form of disease.

• Helps in rehydration of skin, decreasing skin dryness. Replaces essential fatty acids locally.

• Increases skin elasticity. Decreases tension and itch of skin. Cleaning effect.

• Daily min. 2x in case of symptoms and 1x daily for preventive reasons

• Whole body use

Emollient therapy in AD

• Emollients right after shower (~5 min; ~27 Celsius), after gentle drying (skin still moist). • Long effect even without shower. • Allergens in emollients must be avoided to prevent sensitization via skin.

• By its water-binding elements (e.g. urea, glycerol, hyaluronic acid) it hydrates stratum corneum • Occlusive characters (lipid, fat, oil contain) TEWL decreases • Further effects: changes microbiome and pH; increases AMP level; FLG and loricrin expression increases; T cell and DC infiltration decreases; antifungal, anti-pruritic, anti-inflammatory effects

FLG: filaggrin; TEWL: transepidermal waterloss; AMP: antimicrobial peptide Wollenberg és mtsai 2003; Boussault és mtsai 2007; Chiang & Eichenfield, 2009 Skin diseases in wrestling

• Trauma

• Eczema (contact dermatitis)

• Infection (fungal, bacterial, viral, parasitic) Contact dermatitis • Heterogeneous group • Noninfectious inflammatory dermatoses in which the the pathological changes in the epidermis and the upper dermis produce distinctive clinical pictures • Extremely common, 15-25% of patients with skin diseases • Occupational dermatosis (No1) Classification of eczemas

Exogenous agents and Exogenous agents genetic susceptibility

Dermo-epidermal Dermo-epidermal barrier Id-reaction barrier and immunological mechanisms

Irritant Allergic contact Asteatotic eczema contact dermatitis dermatitis Dyshidrosis

Chronic cummulative Mikrobial eczema irritant eczema

Hyperkeratotic Nummular eczema handand foot eczema

Pityriasis simplex Seborrheic eczema

Dermatitis glutealis Atopic dermatitis infantum

Intertrigo Intertriginosus eczema Special forms Treatments in general

• Conventional medicine must be recommended and prescribed by physicians or health care professionals.

• Wrestlers not reporting a skin condition/infection and using unusual and unhealthy treatments (e.g. nail polish remover, bleach, salt, vinegar solutions) are causing unwanted adverse events (e.g. suffocate or burn an infection, leaving extensive scars).

• ”Home remedies” – may be successful, but do not guarantee to kill the infection (only eliminating visible symptoms temporarily). Thus infections may not be symptomatic, but still remain transmittable. Contact dermatitis – treatment

• Define etiology, classification • Eliminate provoking factors • Restore epidermal barrier function • Moisturize • Anti-inflammatories, immunosuppression (topical corticosteroids, topical calcineurin inhibitors)

Acronym: DERMA (skin) Skin infections in wrestling

10% of time-loss injuries in wrestling are due to skin infections

By National Collegiate Athletic Association's (NCAA) Injury Surveillance System • Fungal • Bacterial • Viral • Parasitic

• Overall skin infection rate 14/10000 • 22% recurrence rate • Rate for viral infections was 1.7x the rate of bacterial and 2.1x the rate of fungal infections

NCAA GUIDELINE 2j Skin Infections in Athletics 2008 Herzog MM et al J Athletic Training 2017; 52:457-63. Skin infections in wrestling

• Fungal • Bacterial • Viral • Parasitic

• Direct contact • Indirect sources (mats, headgear, towel, uniform) • In scalp may get deeper lesions • Tinea corporis gladiatorum; • Athletes foot; jock itch; ringworm Fungal skin infections treatment

• Topical – cream, ointment – Once a day; – Do not cover; – 7-10 days

• Systemic – tablets, capsules – Extent forms of disease – Scalp involvement – Until total clearance (weeks)

• Combination • In recurrent cases antifungal prevention may be possible

Skin infections in wrestling

• Folliculitis, impetigo, erysipelas, cellulitis • Fungal • Streptococcus pyogenes; Staphylococcus • Bacterial aureus; Pseudomonas • Contagious (crust covered erosions) • Viral • Itch • Parasitic • Direct contact • Predisposing factors (shaving, haircut, eczema), primary sites (head, extremities) Bacterial skin infections treatment

• Topical – cream, ointment – Topical antibiotics, disinfectants – Once a day; – Remove crust; – Cover; – 7-10 days

• Systemic – tablets, capsules – Antibiotics (in prevention not possible – resistance) – Extent forms or systemic symptoms – 7-10 days

• Combination

Community Associated Methicillin Resistant Staph. Aureus (CA-MRSA)

• Looks identical to other forms of S. aureus, but different strains. Irresponsive to regular antibiotics (e.g. Penicillin), but not multidrug-resistant • Seen in community; believed due to antibiotic abuse/overuse for ear infection or viral infections • Very invasive and destructive to skin and soft tissue • Can spread to the lungs causing serious pneumonia • Can only be diagnosed by culturing an infection • When it occurs, usually seen as an abscess or boil (59%) vs cellulitis (42%) or folliculitis (7%) • Primarily seen in contact sports (wrestling, rugby) • Clindamycin (4x300mg) for 10 days; incision and drainage

B.J. Anderson, M.D.; Boynton Health Service University of Minnesota; Team Physician for Augsburg College Wrestling Team Skin infections in wrestling

• Fungal • Latent virus (cluster) • Bacterial • Contagious (30% chance to contract) (vesicles, open sores, early crusts) • Viral – herpes • HSV-1, HSV-2 • Parasitic • Painful • Lips, body, genitals • Recurrence (stress, immuncompromised) • Secondary bacterial superinfection Skin infections in wrestling

• Fungal • Herpes gladiatorum • Bacterial • Prevalence: 3-20% (varies in age groups) • Viral – herpes • Primary outbreak: malaise, pharyngitis, • Parasitic fever, lymphadenopathy • Primarily at ”lock-up” position: 70% head and face; 40% extremities; 30% trunk • Skin-to-skin contact • 3-8 days after contact, lasts for about 10 days • All wrestlers in contact with it, should be isolated and monitored for 8 days. If no lesions develop, return to competition

www.medscape.com

B.J. Anderson, M.D.; Boynton Health Service University of Minnesota; Team Physician for Augsburg College Wrestling Team Herpes infection – treatment

• Topical – cream, ointment – Not so effective • Systemic – Acute – Start within 3 days – Acyclovir 5x200mg for 7-10 days (even longer) • Systemic – Recurrence – Min 3x in 6 months – Acyclovir 2-3x200mg or 2x400mg for 6 months • Preventative antiviral medication may be possible starting five days before the season and continuing throughout the season. Prophylactic valacyclovir (QD 1g) for 1M in wrestlers resulted in 85% decrease in the probability and 90% decrease in the incidence of outbreak. Skin infections in wrestling

• Fungal • HPV; Pox virus • Bacterial • Direct contact • Contagious until removed • Viral – wart, molluscum • Parasitic Wart/molluscum infection – treatment

• Topical – exfoliative – Salicylic acid • Topical – cytostatic – Podophyllum • Topical – immunomodulatory – Imiquimod

• Surgical – Liquid nitrogen – Electrosurgery – Curettage – Laser (ablative) Skin infections in wrestling

• Fungal • Direct contact • Bacterial • Intense pruritus • Predilection areas (neck, hands, genitals) • Viral • Contagious until treated (STI!) • Parasitic – • Eczema remains scabies, lice • Possible superinfection • Benzyl benzoate; Permethrin

Pediculus humanus capitis Sarcoptes scabiei (mite) Guidelines for Infected Athletes

• Appropriate treatment (3-5-14 days depending on the disease)

• No new lesions present (for 2-3 days)

• Proper bandage (cover)

NFHS: National Federation of State High School Associations; NCAA: National Collegiate Athletic Association; NATA: National Athletic Trainers Association; AAP: American Academy of Pediatrics

Davies HD et al. Pediatrics 2017;140(4):e20172477 Preventions in skin infections

• Utilize recommended procedures for cleaning and disinfection of surfaces. Clean workout gear, clothes, towels for each practice. Mats must be cleaned before each practice with appropriate disinfectant. • Regular skin check (performed every day before practices) (visual enough no palpation necessary) • Improve wrestlers’ hygiene practices • Shave your face only (otherwise opportunity for infection) • Wrestlers must shower immediately after practice (nearly 10% do not do!) • Coaches and trainers must be educated on skin infections

Prevention Key to Reducing Skin Infections in High School Wrestling by B.J. Anderson, M.D., and Larry Cooper, MS, LAT, ATC on December 21, 2015 Skin examination and rules

• At wrestling meets, skin must be checked by medical experts or trained referees. • Any skin condition must be stated non-infectious, adequately medicated and covered with bandage. • Wrestlers must have developed no new lesions 72 hours prior to examination. • Open wounds and infectious skin conditions that cannot be adequately protected are considered grounds for disqualification (from both practice and competition). • Wrestlers undergoing treatment must provide written documentation from a physician (diagnosis; culture results - if possible; date therapy began; names of medications.

National Collegiate Athletic Association's (NCAA) Injury Surveillance System Conclusion – Take home message

• Skin infections may be significant problems in wrestling • Look after your environment (clean equipment)! Protect yourself of harm/danger (danger model)! • Keep the barrier intact! Prevention by moisturizing • Prompt and proper diagnosis by specialist dermatologist inevitable in case of dermatological disorders • Isolation and observation of individual • Targeted treatment if necessary (avoid ”home remedies”) • Importance of withdrawal of wrestler’s permission from competition